Systemic Pathology

Front 1

What is the A-a gradient?

Back 1

It is the difference between the alveolar Po2 and arterial Po2 (they are never the same)

Front 2

When do we Calc the A-a gradient? What are you looking for?

Back 2

A-a gradient is calculated when dealing with a Px with Hypoxemia.

It is used to determine whether Hypoxemia is d/t pulmonary or extrapulmonary causes

Front 3

While standing where is Ventilation/Perfusion greatest in the lungs?

Back 3

Ventilation=greatest at the Apex of the lungs (explains why TB greatly affects this region b/c its an aerobic pathogen)

Perfusion=greatest in the lower lobes (explain why Intrapulmonary infarcts occurs most at this region)

Front 4

What determines a pulmonary involvement of Hypoxemia?

Back 4

Px has hypoxemia with an INCREASED A-a gradient

Front 5

What determines an extrapulmonary involvement of Hypoxemia?

Back 5

Px has hypoxemia with a NORMAL A-a gradient
(ex. Respiratory acidosis)

Front 6

What is the equation for Calc A-a gradient?

Back 6

PAo2=% o2 (713) – arterial Pco2/0.8

Nm % o2= .21
Nm arterial Pco2=40

Front 7

What is a normal value of A-a gradient?

Back 7

Nm A-a gradient= 5mm Hg (PAo2=100mmHg; Pao2=95mmHg; 100-95=5)
A-a gradient= equal/greater than 30: Is medically significant; gives us a + predictive value (there’s truly something wrong)

Front 8

What are some causes of hypoxemia with an INCREASED A-a gradient? (lung-related)

Back 8

Ventilation defect: impaired o2 delivery to the alveoli for gas exchange (ex. Airway collapse d/t RDS)

Perfusion defect: decreased/absent blood flow to alveoli (ex. Pulmonary embolus)

Diffusion defect: o2 is unable to pass thru alveolar-capillary interface (ex. Interstitial fibrosis, pulmonary edema)

Right-to-left cardiac shunt (ex. Tetralogy of Fallot)

Front 9

What are some causes of hypoxemia with a NORMAL A-a gradient? (non-lung related)

Back 9

Depression of respiratory center in the medulla (ex. Barbiturates, Brain injury)

Upper airway obstruction d/t:

Café coronary (food blocking airway)

Epiglottitis d/t H. Influenza

Croup d/t ParaInfluenza virus (narrows the trachea)

Chest bellows (muscles of respiration) dysfunction d/t:

Paralyzed diaphragm

ALS with degeneration of anterior horn

Front 10

what are nasal polyps?

Back 10

They are non-neoplastic tumefactions that develop as a response to chronic inflammation

Front 11

Characteristics of Allergic polyps?

Back 11

-most common polyp
-usually ONLY associated with ADULTS with a history of IgE-mediated allergies

Front 12

Describe the occurrence of nasal polyps in people taking Aspirin/NSAIDS?

Back 12

-usually involves a female with chronic pain (fibromyalgia)
Presents a clinal triad:
-Aspirin (NSAIDS)
-Asthma
-Nasal polyp

Front 13

Describe the pathogenesis of Nasal polyps seen in people taking Aspirin (NSAIDS)?

Back 13

Aspirin blocks the cyclooxygenase leaving the lipoxygenase pathway open

Leukotrienes (LT C,D,E4) are increased causing bronchoconstriction which leads to asthma

Front 14

What do you do when you see a nasal polyp in a child?

Back 14

-order a SWEAT TEST to rule out CYSTIC FIBROSIS

Nasal polyps are usually not seen in normal children

Front 15

Characteristics of Laryngeal Carcinoma?

Back 15

-It's more common in men than women
-usually located on the TRUE VOCAL CORD
-majority are keratinizing squamous cell carcinomas

Front 16

What are the causes of Laryngeal Carcinoma?

Back 16

-cigarette smoking (most common cause)
-alcohol (has a synergistic effect with smoking)
-squamous papilloma/papillomatosis (HPV 6/11)

Front 17

What are the clinical symptoms associated with Laryngeal Carcinoma?

Back 17

Persistent hoarseness often associated with cervical lymphadenopathy

Front 18

What is Atelectasis? What are the 3x ?

Back 18

Refers to the collapsing of airways
1. Resorption atelectasis
2. Compression atelectasis
3. Atelectasis d/t loss of surfactant (RDS in babies)

Front 19

What is the pathogenesis of Resorption atelectasis?

Back 19

Involves airway obstruction preventing air from reaching the alveoli

Obstruction occurs in:
Bronchi
Segmental bronchi
Terminal bronchioles

Front 20

Causes of obstruction in Resorption atelectasis?

Back 20

1. Mucus or mucopurulent plug after surgery
2. Aspiration of foreign material
3. Centrally located bronchogenic carcinoma

Front 21

What are the clinical finding associated with Resorption Atelectasis?

Back 21

Fever and Dyspnea (24-36hrs after collapse)
Decreased percussion (absent breath sounds)
Increased tactile fremitis (vocal vibratory sensation)
Ipsilateral ELEVATION of DIAPHRAGM
Ipsilateral TRACHEAL DEVIATION
INSPIRATION LAG (collapse lung does not expand on inspiration)

Front 22

Characteristics of Spontaneous Pneumothorax?

Back 22

-usually seen in tall males or squba divers
Clinical findings:
Ipsilateral ELEVATION of DIAPHRAGM
Ipsilateral TRACHEAL DEVIATION

Front 23

What is the most common cause of Spontaneous Pneumothorax?

Back 23

Ruptured subpleural blebs leaving holes in the lungs (air pockets)

Leads to a change in negative intrathoracic pressure causing alveoli to collapse

Front 24

Characteristics of Compression atelectasis? And clinical findings?

Back 24

Involves air/fluid under pressure in the pleural cavity collapses small airways beneath the pleura

Clinical findings:
Trachea deviates the contralateral side
No elevation of the diaphragm

Front 25

What are some examples of Compression atelectasis?

Back 25

Tension Pneumothorax (air compressed lung)
Ex. Knife injury

Pleural effusion (fluid compressed lungs)

Front 26

Difference between a spontaneous/tension Pneumothorax?

Back 26

Spontaneous:
-d/t Resorption atelectasis
-Ipsilateral ELEVATION of DIAPHRAGM
-Ipsilateral TRACHEAL DEVIATION

Tension:
-d/t Compression atelectasis
-Trachea deviates the contralateral side
-No elevation of the diaphragm (down)
-mediastinal shift

Front 27

Where is surfactant made?

Back 27

-they are made by TYPE II PNEUMOCYTES
-stored in lamellar bodies
-synthesis usually begin in 28th week of gestation

Front 28

What is the function of surfactant?

Back 28

-reduces surface tension in small airways
-prevents collapse of airways on expiration

during expiration:
collapsing pressure is greatest:
CP=2T (surface tension)/ r (radius of alveoli)

Front 29

What are some things that affect the synthesis of Surfactant?

Back 29

Increase synthesis:
1. Cortisol (glucocorticoid)
2. Thyroxine
3. Prolactin

Decrease synthesis:
1. Insulin

Front 30

Pathogenesis of Respiratory Distress Syndrome in newborns?

Back 30

1. Decrease surfactant in the fetal lungs
2. Widespread atelectasis results in massive intrapulmonary shunting (ventilation defect: AKA perfusion w/o ventilation)

Front 31

What are the three main causes of decreased surfactant in newborns with RDS?

Back 31

1. Prematurity
2. Maternal diabetes (fetal hyperglycemia increases insulin release)
3. Cesarean section

Front 32

What is the recommended procedure for women have to deliver their babies prematurely?

Back 32

Administration of glucocorticoids in order to increase fetal surfactant and reduce the chances for RDS

Front 33

Why do women with high glycemic index have big babies during delivery?

Back 33

If mother is hyperglycemic then the baby is as well while in her stomach

However, when the umbilical cord is cut and the baby is delivered the baby is no longer hyperglycemic, but still has high amount of insulin in the circulation which leads to:
-increase fat storage in adipose tissue
-increase synthesis of triglycerides
-increase amino-acid in muscle->Increase muscle mass

Front 34

What causes the presence of HYALINE MEMBRANE seen in the RDS of newborns?

Back 34

-they are derived from proteins leaking out of damaged pulmonary vessels

Front 35

What are some symptoms associated with RDS in newborns?

Back 35

-respiratory difficulty with a few hours after birth
-Infant develops HYPOXEMIA AND RESP. ACIDOSIS
-chest radiograph shows a "GROUND GLASS" appearance

Front 36

What are some of the complication of RDS in newborns?

Back 36

1. Superoxide free radical damage from o2 therapy
(blindness/bronchopulmonary dysplasia)
2. Intraventricular hemorrhage
3. Patent ductus arteriosus (d/t HYPOXEMIA)
4. Necrotizing enterocolitis
(Intestinal ischemia allows entry of gut bact. into intestinal wall)
5. Hypoglycemia in newborn

Front 37

What causes Hypogllycemia in newborns with RDS?

Back 37

the excess insulin from their fetal hyperglycemia decreases serum glucose producing seizures and damage to neurons

Front 38

How do you treat RDS in newborns?

Back 38

PEEP therapy (Postive-end-expiratory Pressure)
-is the pressure added to the lung above atm pressure
it opens up the collapsed airway allowing surfactant to be delivered

Front 39

What is the most common cause of Acute respiratory distress syndrome (ARDS)?

Back 39

Septic Shock (Gram - sepsis)
progression:
Sepsis--->ARDS--->DIC--->DEATH

Front 40

Characteristic of ARDS?

Back 40

Is a life-threatening reaction to injury of the lung or systemic diseases

causes noncardiogenic pulmonary edema resulting from acute alveolar-capillary

Poor prognosis (~60% mortality rate)

Front 41

What are the risk factors of ARDS?

Back 41

1. Gram- sepsis (40% of cases)
2. Gastric aspiration (30% of cases)
3. Severe trauma with shock (10% of cases)
4. Diffuse pulmonary infection, heroin, smoke inhalation

Front 42

What immune agent cause the damage seen in ARDS

Back 42

Neutrophils
- it damages both types I and II pneumocytes
(decreasing surfactant causing atelectasis with intrapulmonary shunting)

Front 43

What is the 1st phase of ARDS pathogenesis?

Back 43

-cytokines are released that are chemotactic to neutrophils
- neutrophils transmigrate into the alveoli through pulmonary capillaries
- capillary damage causes leakage of protein-rich exudate producing HYALINE MEMBRANES

Front 44

What is the 2nd phase of ARDS pathogenesis?

Back 44

Damage of Type 1+2 pneumocytes by Neutrophils

Front 45

What is the 3rd phase of ARDS pathogenesis?

Back 45

Repair by Type II pneumocytes

Progressive interstitial fibrosis (restrictive lung disease)

Front 46

What are some of the symptoms of ARDS?

Back 46

1. Dyspnea with severe hypoxemia that is not responsive to o2 therapy

2. Acute respiratory acidosis

Front 47

What are the 2 different types of Pneumonia?

Back 47

1. Community-acquired
a. Typical
b. Atypical

2. Nosocomial (hospital-acquired)

Front 48

Characteristics of Typical community-acquired pneumonia?

Back 48

-majority are caused by bacteria
(most often d/t Strep. pneum.)
2x:
1. Lobar pneumonia
2. Bronchopneumonia

Front 49

Pathogenesis of Typical community-acquired pneumonia?

Back 49

1. Inhalation of aerosol (solid particles, liquid droplets) from an infected individual

2. Aspiration of nasopharyngeal flora while sleeping
(Strep. mutant, pyogenes, salivarius, Neisseria)

Front 50

Characteristics of bronchopneumonia?

Back 50

-usually begins as an acute bronchitis and eventually spreads into the lungs
-Usually involves the lower lobes or right middle lobe
-LUNGS HAS PATCHY AREAS OF CONSOLIDATION
(presence of microabscesses in area of consolidation)

Front 51

What is the difference between Lobar pneumonia and bronchopneumonia on chest radiograph?

Back 51

(GOLD STANDARD SCREEN)
Lobar:
appears as complete or almost complete consolidation of the lungs

Bronchopneumonia:
usually seen as patchy areas of consolidation

Front 52

What are some complications of Pneumonia?

Back 52

1. Lung abscesses
2. Empyema (pus in the pleural cavity)
3. Sepsis

Front 53

What are some of the symptoms of Typical Community-acquired Pneumonia?

Back 53

1. Sudden onset of high fever with productive cough
2. Signs of consolidation (alveolar exudate)

Front 54

What are some of the diagnostic findings the consolidation seen in Typical C-A pneumonia?

Back 54

1. Dullness to percussion
2. Increased vocal tactile fremitis
3. Inspiratory crackles (air moving through exudate in the alveoli)
4. Egophany (E-->A sign)
5. Whisper pectoriliquy

Front 55

How does Pneumonia differ from Pleural effusion?

Back 55

Effusion only has dullness to percussion and does not show any other diagnostic findings

Front 56

What are the lab finding of Typical C-A pneumonia?

Back 56

1. Positive Gram stain
2. Neutrophil Leukocytosis

Front 57

What are the microbes responsible for Atypical C-A pneumonia?

Back 57

1. Mycoplasma pneumonia (MCC)
2. Chlamydia pneumonia (TWAR AGENT)
3. Chlamydia trachomatis (newborns)
4. Viruses:
RSV
Influenzavirus
Adenovirus

Front 58

How can someone contract atypical C-A pneumonia?

Back 58

It can be contracted by inhalation of droplets (infected droplet)

Front 59

What are the lab findings of atypical C-A pneumonia?

Back 59

Patchy interstitial pneumonia:
1. Mononuclear infiltrate
2. Alveolar space are usually free of exudate (reason for non-productive cough)

Front 60

What are the symptoms associated with Atypical C-A pneumonia?

Back 60

1. Insidious onset low-grade fever
2. Non-productive cough
3. No consolidation
4. Flu-like symptom:
Pharyngitis, Laryngitis, myalgias, headaches

Front 61

What are some of the microbes responsible for Nosocomial Pneumonia?

Back 61

Gram- bacteria:
1. Pseudomonas aeruginosa (respirators)
2. E. coli

Gram+ bacteria:
1. Staph. aureus

Front 62

What are some of the causes of Nosocomial pneumonia?

Back 62

Respirators (MCC)
Antibiotic therapy
Immunosuppression
Severe underlyinig disease

Front 63

What are some immunocompromised states in which pneumonia is a major complication?

Back 63

1. AIDS
2. Bone marrow transplants

Front 64

What are some opportunistic pathogens that cause pneumonia in immunocompromised patients?

Back 64

1. Cytomegalovirus (CMV)
2. Pneumocystis jiroveci (Trimethoprim-sulfamethoxazole for prophylaxis and treatment)
3. Aspergillus fumigatus